The primary objective of this research is to further our understanding of biobehavioral mechanisms which may contribute to the increased incidence of cardiovascular disease in postmenopausal compared to premenopausal women. Evidence suggests that estrogen alters stress responses in ways which reduce the putative impact of stress in the pathogenesis of cardiovascular disease. Thus, in post-menopausal women the "protective" effects of estrogen during stress may be lost. The present proposal will focus on the impact of estrogen on hemodynamic responses that may promote the development of hypertensive heart disease and on lipid responses that may favor atherogenesis. The role of estrogen on hemodynamic, catecholamine and lipid responses during stress will be examined in: (i) a cross-sectional comparison of 140 premenopausal with 70 post-menopausal women; (ii) a follow-up study of 90 women, evaluating response changes in premenopausal women who become menopausal, and in early postmenopausal women who are retested 3 years later. The role of adrenergic receptor mechanisms in the heart and vessels during the progression through menopause will be examined in a subsample of 60 women. Ambulatory blood pressures and echocardiographic measures of left ventricular structure will also be collected on all subjects. The data from these studies will permit testing of hypotheses, generated by a Biobehavioral Model of Heart Disease, that targets mechanisms by which estrogen depletion following menopause may increase cardiovascular morbidity and mortality.